Abstract: In one individual, who developed a transient increase in CSF HIV-1 RNA, seven of seven CSF and plasma clones had identical enfuvirtide resistance-associated V38A mutations, suggesting that the CSF quasispecies derived from that of blood.
Specific enfuvirtide-associated mutational pathways in HIV-1 Gp41 are significantly correlated with an increase in CD4(+) cell count, despite virological failure.
PMID: 18419549
2008
The Journal of infectious diseases
Abstract: Residues 38 and 18 are located complementarily to each other in the Rev-responsive element, whereas analysis of molecular dynamics showed that the copresence of [V38A + N140 I] abolishes the interaction between residue 38 and 145 important for stabilization of the 6-helix bundle.
Abstract: The ENF-associated clusters [V38A + N140I ] and [V 38A +T18A ] significantly correlated with an increase in CD4 cell count at week 48 ( an increase from baseline of 112 and 209 cells/microL, respectively), whereas [Q40H + L45M + 268A] significantly correlated with a decrease in CD4 cell count (-53 cells/microL), without a change in the level of viremia.
HIV-1-infected patients from the French National Observatory experiencing virological failure while receiving enfuvirtide.
PMID: 18552344
2008
The Journal of antimicrobial chemotherapy
Abstract: In the HR-1 domain, the V38A/M, Q40H, N42T, N43D and L45M mutations wereselected (P < 0.02).
Viral dynamics and in vivo fitness of HIV-1 in the presence and absence of enfuvirtide.
PMID: 18645515
2008
Journal of acquired immune deficiency syndromes (1999)
1Abstract: Subsequently, ENF was readministered for 4 weeks as ""pulse intensification."" METHODS: The proportion of plasma virus carrying the V38A mutation in gp41 was quantified by allele-specific real-time polymerase chain reaction in serial samples collected from 3 subjects at 1- to 4-week intervals."
Abstract: RESULTS: The V38A mutant made up >or=85% of the quasispecies at baseline and decayed to <5% over 12-24 weeks; plasma HIV-1 RNA levels remained stable during this time.
Abstract: The V38A mutant virus reemerged rapidly during the ENF pulse.
Abstract: The relative stability of plasma HIV-1 titers during decay of V38A suggests that factors other than viral fitness likely define viral load set-point in patients with advanced disease.
Introduction: The
Role of the HIV gp120 conserved domain 1 in processing and viral entry.
PMID: 18815131
2008
The Journal of biological chemistry
Abstract: Based on Western blot analyses of cell lysates and virions, the entry impairment of W35A, V38A, Y39A, Y40A, G41A, V42A, and I52A is due primarily to disruption of envelope processing.
Peptide P5 (residues 628-683), comprising the entire membrane proximal region of HIV-1 gp41 and its calcium-binding site, is a potent inhibitor of HIV-1 infection.
Method: The envelope proteins of the two other viruses, T20-1 and T20-2, as well as the virus populations from which they were derived, expressed the V38A resistance mutation.
Systematic evaluation of allele-specific real-time PCR for the detection of minor HIV-1 variants with pol and env resistance mutations.
PMID: 17662474
2007
Journal of virological methods
Abstract: The assays achieved sensitivities of <1% for the D30N mutation in HIV-1 PR, M184V and I mutations in RT, and V38A in gp41.
Specific mutations in HIV-1 gp41 are associated with immunological success in HIV-1-infected patients receiving enfuvirtide treatment.
PMID: 16891628
2006
The Journal of antimicrobial chemotherapy
Abstract: V38A/E were the most represented mutations at all time-points.
Abstract: CONCLUSIONS: Specific enfuvirtide resistance mutations (V38A/E) are associated with a sustained CD4 increase, without remarkable effects upon viraemia.
Abstract: The presence of V38A/E was significantly associated with a 4.5-fold CD4 increase from baseline to week 24 and with a 6-fold increase at week 36 (P = 0.004 and 0.02 compared without V38A/E, respectively), without significant correlation with viraemia.
Rapid emergence of enfuvirtide resistance in HIV-1-infected patients: results of a clonal analysis.
PMID: 16885776
2006
Journal of acquired immune deficiency syndromes (1999)
Abstract: Mutations at codons 36 (G36E, G36D, or G36S) and 38 (V38A, V38G, or V38M) were the most commonly detected resistance mutations at week 2.
HIV mutation literature information.
PMID: 
2009
AIDS research and human retroviruses
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